MUC5AC drives COPD exacerbation severity through amplification of virus-induced airway inflammation

Aran Singanayagam; Joseph Footitt; Benjamin T Kasdorf; Matthias Marczynski; Michael T Cross; Lydia J Finney; Maria-Belen Trujillo Torralbo; Maria Calderazzo; Jie Zhu; Julia Aniscenko; Thomas B Clarke; Philip L Molyneaux; Nathan W Bartlett; Miriam F Moffatt; William O Cookson; Jadwiga Wedzicha; Christopher M Evans; Oliver Lieleg; Patrick Mallia; Sebastian L Johnston

The copyright holder for this preprint (which was not peer-reviewed) is the . https://doi.org/10.1101/706804 doi: bioRxiv preprint and found that sputum MUC5AC concentrations during virus-induced exacerbations also correlated with bacterial loads in the 2 week sample during exacerbation, as the peak of secondary bacterial infections occurs around 2 weeks after virus infection 16 (Supplementary Fig.2a) . Although not induced during infection at any time point assessed, similar analyses were carried out for MUC5B. However, in contrast to MUC5AC, MUC5B did not significantly correlate with any inflammatory marker except GM-CSF (Supplementary Fig.1d) . Similarly, there were no significant correlations of MUC5B with virus load (Supplementary Fig.1e) , and changes from baseline in antimicrobial peptide concentrations (Supplementary Fig. 1f) or bacterial loads during experimental (Supplementary Fig.1g ) or naturally-occurring ( Supplementary Fig.2b ) COPD exacerbation.